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Function of the Heart

  • Functions via calcium binding to troponin, which causes tropomysin to move and exposes myosin binding sites on the actin filament, allowing ATP mediated contraction to occur

   Figure 1: The Cardiac Troponin-Actin-Myosin Complex

  • The function of the heart can be described by Pressure-Volume Loops which consist of 2 curves: End Systolic Pressure Volume Relationship (ESPVR) and End Diastolic Pressure Volume Relationship (EDPVR)
  • ESPVR is analogous to the Frank-Starling relationship which describes increasing force generated by a muscle fiber when stretched. Hence, surrogate measures can be used for "stretch" such as preload, end diastolic pressure, or end diastolic volume while surrogate measures can be used for "force" such as stroke volume, cardiac output, etc. 
  • Changes in inotropy shift the ESPVR curve left with increases in inotropy and rightwards with decreases in inotropy (Figure 3)
  • Changes in lusitropy, or the compliance/diastolic function/ability of the heart to relax, shift the EDPVR curve, rightwards with increased compliance (ie with Milrinone) or leftwards with decreasing compliance (Figure 4)

Figure 2: The LV Pressure and Volume curves over time (left) as well as the LV Pressure/Volume Loop     


                     Figure 3: Starling Curves                 Figure 4: LV Diastolic Curve                            Figure 5: Putting the Two Together

Interpreting the CVP waveform

Figure 6: The CVP Waveform

The normal CVP waveform (Figure 6) consists of various waves: 
    1) a wave: due to atrial contraction at the end of diastole
    2) c wave: due to the tricuspid valve bulging into the RA during isovolumic contraction
    3) x descent: due to atrial relaxation as the ventricle contracts
    4) v wave: due to filling of the atrium during systole
    5) y descent: due to emptying of the atria into the ventricle during diastole 

Various pathological processes can alter the CVP waveform:

    1) canon a waves:  large a waves seen with AV dissociation (ie JET) as the atrium contracts against a closed tricuspid valve
    2) loss of a waves: occurs in atrial fibrillation as there is no longer a significant atrial contraction
    3) prominent CV wave: occurs with tricuspid regurgitation; as the ventricle contracts, the regurgitation causes an increase in the C and V waves

Figure 7: Pressure, Volume EKG, Heart Sounds over the Cardiac Cycle


  • Acute or subacute, occurs when fluid or blood builds up in the pericardial space
  • Typically, the pericardial space can accommodate shifts in intracardiac volume. However, as fluid accumulates in the pericardial space, the capacity to accommodate reaches an inflection point and the pressure rapidly rises, reducing cardiac filling

Pericardial compliance and capacity varies depending on whether the effusion has accumulated rapidly or slowly

  • Physiology: Ventricular interdependence, meaning as the RV fills with inspiration, because the free wall is restricted due to the pericardial fluid, the only direction for filling to occur is towards the septal wall, thereby inhibiting LV filling and subsequent stroke volume and pulse pressure 

  • Clinical Signs: Classically described Beck's Triad (Muffled heart sounds due to effusion, jugular venous distension, and hypotension due to impaired filling) seen in a minority of cases

  • Tachycardia may be the only sign in many patients before more significant decompensation
  • May also see pulsus paradoxus
  • Echo findings: Pericardial fluid, can also see RA and RV collapse on echocardiography but important to note that cardiac tamponade is a clinical diagnosis, not an echocardiographic diagnosis
  • Treatment: pericardial drainage via pericardiocentesis, potentially with placement of a pericardial drainage catheter

Treatment of Hemodynamic Dysfunction

Fundamentally, Ohm's Law states: Voltage= Current X Resistance. This can be applied to hemodynamics in that: Change in pressure = Flow X Resistance.

Hence, for systemic hemodynamics: 

Systemic blood pressure = CO X Systemic Vascular Resistance (SVR)


For any state of hypotension, it is either an issue with cardiac output and/or systemic vascular resistance. Typically, the body will compensate for the perturbation by increasing the other component.

For example: 

1) Decreased cardiac output (ie cardiogenic shock, hypovolemia, bradyarrythmia, etc), the body compensates for low CO by increasing SVR to try and maintain BP. Hence, the patient looks clamped down with poor peripheral perfusion and capillary refill. This is COLD SHOCK. You want to augment cardiac output in this situation (via fluid for increased preload, inotropy for poor contractility, chronotropy for bradyarrhythmias, etc) and perhaps even reduce SVR (decrease afterload) on the stressed heart. The patient is already vasoconstricted and so vasopressor agents that further SVR are less useful in this circumstance (and perhaps even harmful). 

2) Decreased SVR (ie anaphylaxis, distributive shock), the body compensates for low SVR by increasing CO. Hence, the patient is hyperdynamic, has flash capillary refill and bounding pulses. This is WARM SHOCK. You want to use agents (ie norepinephrine) that will increase SVR. The patient is likely already hyperdynamic so inotropic (B1) agents are less useful in this circumstance. 

  • Treatment consists of treating the underlying etiology (bleeding, hypovolemia, sepsis, etc)
  • Fluids are given for augmenting preload to take advantage of the Frank-Starling relationship
  • Vasoactive agents are used to augment SVR or cardiac output, depending on the pathophysiology (see below)

Figure 8: Common Vasoactives and Their Effects

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